The effects of some inhalation anaesthetics on the sodium current of the squid giant axon.

Haydon, D. A.; Urban, B. W.

doi:10.1113/jphysiol.1983.sp014814

Cited by 104 publications

(49 citation statements)

References 18 publications

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“…The observed changes in the threshold level are compatible with the effects on the Na+ current of squid axons. The anaesthetics shifted the steady-state inactivation curve in the hyperpolarizing direction while the steady-state activation was shifted in the depolarizing direction (Haydon & Urban, 1983). Regardless of how the anaesthetics depress the IPSPs, the after-hyperpolarization and the PTH, the elevation of the threshold for spike generation induced by the anaesthetics would result in a decrease of neuronal excitability.…”

Section: Discussionmentioning

confidence: 99%

Changes in spontaneous firing patterns of rat hippocampal neurones induced by volatile anaesthetics.

Fujiwara

Higashi

Nishi

et al. 1988

The Journal of Physiology

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SUMMARY1. The effects of the volatile anaesthetics, halothane, isoflurane and enflurane, on rat hippocampal CAI and CA3 neurones in in vitro preparations were studied by intracellular recording methods.2. The three anaesthetics, at concentrations similar to those used clinically (02-1-2 mM), initially increased and then subsequently decreased the spontaneous firing of CAI neurones without affecting the resting membrane properties or the EPSPs evoked by focal stimuli.3. The anaesthetics at these concentrations depressed both the fast afterhyperpolarization of the soma spike and the post-tetanic hyperpolarization induced by repetitive stimulation. They also decreased the IPSPs evoked by focal stimuli.4. The threshold for spike generation was gradually elevated by as much as 4-6 mV during application of the anaesthetics at these concentrations. The subthreshold potential oscillations (which are likely to be associated with periodic alterations in non-inactivating Ca2+ and Na+ currents) were enhanced in the low concentrations (0-2-0-5 mm), but were depressed in the high concentrations (0-8-1-2 mm).5. The results suggest that the transient increase in the firing frequency was caused by a depression of both the spike after-hyperpolarization and the post-tetanic hyperpolarization, and that the reduction of spontaneous firing was mainly due to an elevated threshold for spike generation.6. The three anaesthetics altered the pattern of spontaneous spike-firing in CA3 neurones from solitary spiking to burst firing without affecting the resting membrane properties.7. The effects of the anaesthetics on the active membrane properties and the postsynaptic potentials in CA3 neurones were similar to the effects in CAI neurones.8. In the majority of CA3 neurones, soma spikes elicited by depolarizing current pulses were followed by a Ca2+-dependent after-depolarization, which was in turn followed by a prolonged after-hyperpolarization (post-burst hyperpolarization). The anaesthetics facilitated the after-depolarizing potential, while they depressed the t To whom all correspondence and reprint requests should be sent.

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Section: Discussionmentioning

confidence: 99%

Changes in spontaneous firing patterns of rat hippocampal neurones induced by volatile anaesthetics.

Fujiwara

Higashi

Nishi

et al. 1988

The Journal of Physiology

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“…gNa of axons was not reported to be significantly affected by high concentrations of volatile anesthetics (4-5 mM halothane, 100-200 mM diethyl ether etc. ), and no decrease in the number of the functioning sodium channels was suggested (BEAN et at., 1981;HAYDON and URBAN, 1983c). Shift of the curve in a negative direction was noted in various preparations, with a variety of drugs including general anesthetics (SCHRIVASTAV et at., 1976;BEAN et at., 1981;HAYDON and URBAN, 1983c), local anesthetics (HILLS, 1977a, b;BEAN et at., 1983), hydrocarbones (HAYDON and URBAN, 1983a), alcohols (HAYDON and URBAN, 1983b;HARPER et at., 1983), and barbiturates (SCHWARZ,1979).…”

Section: ) Current Clamp Experimentsmentioning

confidence: 99%

Reduction in the myocardial sodium current by halothane and thiamylal.

et al. 1986

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Effects of two general anesthetics, halothane and thiamylal, on the fast sodium inward current (INa) of enzymatically isolated single rat ventricular cells were studied under current clamp and voltage clamp conditions. A suction pipette technique was used for potential measurement, current injection and internal perfusion of isolated cells. In current clamp experiments, sodium action potential was elicited in a Ca-free Co Krebs solution and the action potential was reduced by 0.5°c halothane and 5 x 10-5 M thiamylal. In voltage clamp experiments, the calcium current was suppressed by replacing Ca with Co and the potassium current was eliminated by replacing K with Cs and adding 4-aminopyridine and tetraethylammonium. Both anesthetics decreased INa, in a dose dependent manner, without changing the shape of the current-voltage curve. Halothane (l°) shifted the steady state inactivation curve in a negative direction along the potential axis by 8.5±2 mV (mean + S.D., n=4). Thiamylal, 5 x 10-5 and 10-4M, shifted the curve in a negative direction by 4.4 ± 0.8 mV (n =5) and 8.6 + 3.2 mV (n = 5), respectively. Both agents slightly reduced the maximum sodium conductance (gNa). Halothane (1 %) increased half recovery time from inactivation measured at -80 mV from 30±15 to 80 + 25 ms (n=4). Thiamylal (104M) -prolonged it at -75 mV from 50± 20 to 110± 15 ms (n=5). With a test pulse duration of 50 ms, neither drug produced a use-dependent inhibition of INa. Halothane and thiamylal depress the INa of cardiac muscles mainly by shifting the steady state inactivation curve in a negative direction along the potential axis. Relatively small prolongation of half recovery time from inactivation and no sign of use-dependent inhibition suggest a molecular mechanism which differs in some respects from the local anesthetics.

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“…Due to the presence of an alcohol group, heptaminol has general anaesthetic properties which can inhibit ionic conductances as shown by Haydon & Urban (1983) important role in depolarization-contraction coupling (Schneider & Chandler, 1973) seems improbable. Indeed calcium channels as dihydropyridine receptors are considered to be the support of these charge movements (Rios & Brum, 1987); the fact that the calcium current is not modified by heptaminol is an indication that charge movements are certainly unaffected.…”

Section: Discussionmentioning

confidence: 99%

Action of heptaminol hydrochloride on contractile properties in frog isolated twitch muscle fibre

Allard

Jacquemond

Lemtiri‐Chlieh

et al. 1991

British J Pharmacology

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1 Heptaminol stopped or delayed the progressive decline in tension which characterizes the phenomenon of fatigue in frog isolated twitch muscle fibre. 2 Heptaminol had no action on the sodium, potassium and calcium voltage-dependent ionic conductances.3 The hypothesis of an action via an internal alkalinization was tested by comparison with the action of NH4Cl. Both substances increased the tension. 4 The action of heptaminol was suppressed in sodium-free (TRIS) solution or in the presence of amiloride while the action of NH4Cl was always observed. 5 These results could be explained by a stimulation of the Na/H antiport by heptaminol.

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The effects of some inhalation anaesthetics on the sodium current of the squid giant axon.

Cited by 104 publications

References 18 publications

Changes in spontaneous firing patterns of rat hippocampal neurones induced by volatile anaesthetics.

Changes in spontaneous firing patterns of rat hippocampal neurones induced by volatile anaesthetics.

Reduction in the myocardial sodium current by halothane and thiamylal.

Action of heptaminol hydrochloride on contractile properties in frog isolated twitch muscle fibre

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